SURGICAL ENCOUNTERS

WITH HEPATOBILIARY
SYSTEM
JEJI.G
Assistant Professor in Surgery
Govt: Medical College
Kottayam
 JEJI.G MS,
Assistant Professor
Dept. of General Surgery

A lucid understanding of
SURGICAL JAUNDICE –
FOR MEDICINE UNDERGRADUATES
BILIRUBIN METABOLISM
Schematic showing the seven steps from formation of
UCB to flow down the biliary tree.
STEP -1 FORMATION
NORMAL SOURCES OF BILIRUBIN

RBC HEMOGLOBIN
1-2 x 10 8 RBC’s 6 grams
per hour
 HEMOGLOBIN (85%)
BONE
MARROW,LIVER
(15%)

GLOBIN

AMINO ACIDS
HEME
AMINO ACID POOL
 HEME
Fe 2+ HEME OXYGENASE

BILIVERDIN
BILIVERDIN
REDUCTASE

BILIRUBIN
Amount of heme broken down to bile
pigments daily

SOURCE AMOUNT LIFE

(turnover)
Senescent 200 mg 120 days
RBC’s
Ineffective 50-100 mg 3 – 7 days
erythropoesis
Cytochrome < 1 day
enzymes
DAILY PRODUCTION OF
BILIRUBIN

250 – 300 mg
(425 – 510 µmol)
STEP – 2 DELIVERY
 BILIRUBIN + ALBUMIN

BILIRUBIN - ALBUMIN
•UCB is tightly (99.9%) bound to plasma albumin
•Cannot filter at the glomerulus or appear in the
urine.
• Conjugated bilirubins are also bound to
albumin, with much lower affinity, allowing the
small unbound fraction to filter at the glomerulus.
 This leads to
bilirubinuria in the
patients with diseases that
cause retention of
conjugated bilirubin
STEP – 3 HEPATIC UPTAKE
STEP – 4 STORAGE
 Only 30% of UCB in
plasma is normally taken
up by the hepatocytes

LIMIT
 BILIRUBIN - ALBUMIN
30% of UCB in plasma is taken up by the hepatocytes

HEPATOCYTE LIGANDIN

BILIRUBIN

BILIRUBIN - LIGANDIN
 STEP – 3, HEPATIC UPTAKE
• 60%bilirubin processed in hepatocyte
• 40% refluxes back to blood
• Hepatic intracellular bilirubin is bound to
LIGANDIN
• Binding  prevents reflux to blood
 storage
• Ligandin GLUTATHIONE-S-TRANSFERASE
• Binding to ‘Z-protein’ also
 STEP – 4 ,STORAGE
• stored temporarily by binding to
several organic-anion binding proteins
(especially ligandin).
• This limits the passive reflux of UCB
back into the plasma
• promotes transfer of UCB to the
smooth endoplasmic reticulum for
conjugation.
STEP – 5 CONJUGATION
 Microsomal conjugation of bilirubin to
form glucuronides

UCB

UCB CB

CB
 BILIRUBIN

UDP GLUCURORYL
UDP-GLUCURONIC TRANSFERASE
ACID
BILIRUBIN MONO GLUCURONIDE
UDP GLUCURORYL
UDP-GLUCURONIC TRANSFERASE
ACID

BILIRUBIN DI GLUCURONIDE
STEP – 6, SECRETION
Microscopic anatomy
ROLE OF TRANSPORTERS

TRANSPORTERS

CB
TRANSPORTERS

TRANSPORTERS
 ROLE OF TRANSPORTERS
• The transport of solute into the
canaliculus by specific transporters
creates chemical and osmotic
gradients and promotes water flow by a
paracellular pathway.
• Several of these specific transporters
have been identified, and their function
has been characterized.
 canalicular transporters

• This transport is stimulated by ATP.

• The proteins include 
bile salt export pump (BSEP)
sister P-glycoprotein (SPGP)
ATP binding cassette sub-family B11
(ABCB11).
ROLE OF TRANSPORTERS
 Bilirubin in the Liver Cell
• Hepatocyte (HC) uptake of UCB
• Alb+UCB dissociates and UCB enters HC
1 • By passive diffusion into HC – Ligandin bound
• Insoluble UCB is to be made soluble in HC

• Conjugation in ER of Hepatocyte (HC)

• Formation of mono and di glucuronides BMG, BDG
2 • UDP Glucuronosyl transferase is energy depend.
• Insoluble UCB made water soluble for excretion

• Excretion in into biliary canaliculi

• Rate limiting step in metabolism
3 • CB 50% is not protein bound – no loss of albumin
• Remaining 50%  bilirubin – Irreversibly bound
Modification of Bile secretion
 Modification of Bile secretion
Bile is modified during its passage along the
biliary ductules by absorption and secretion
of bicarbonate, and limited absorption of bile
salts, glucose and amino acids.

• Water moves passively into the bile by

paracellular and transcellular routes in
response to the osmotic gradients generated
by solute transport.
 Bilirubin in the Intestine
1. CB in bile is excreted into Duodenum
CB 10% diffuses in to blood CB excreted is not reabsorbed

2. Conversion of CB into uro & stercobilinogen

Urobilinogen excreted in stool Part of the UBG enters EHC

3. From gut, UBG but not CB enters EHC

Kidney excretes absorbed UBG In biliary obst. UBG absent in urine
 In the distal ileum and colon,
anaerobic flora mediate further
catabolism of bile pigments
 conjugated bilirubin
hydrolysis
bacterial β-glucuronidases

UCB
multistep
hydrogenation

colorless
urobilinogens Urine
oxidation urobilinogen

brown-colored mesobilifuscins.
Bilirubin handling in Kidney

• Bound (20 days)

Conjugated
Bilirubin • Bilirubin in urine
is conjugated
• Not filtered
Unconjugated or secreted
Bilirubin
• Nil in urine

Urobilinogen • Normally traces

in urine • ↑ in Cholestaiss
 entero-hepatic circulation of
urobilinogens and UCB.
• > 90% of the urobilinogens and
unmetabolized UCB, along with the
mesobilifuscins, are eliminated in the
feces
• entero-hepatic circulation of bile
pigments is limited.
• some urobilinogens are retained and
appear in the urine.
 Contd..

• patients receiving broad-spectrum

antibiotics, have decreased intestinal
UCB degradation
• UCB reabsorption and enterohepatic
recycling are enhanced
• serum levels of UCB are higher.
Bilirubin Metabolism - Summary
 Bilirubin – And its nature

Properties Unconjugated Conjugated

Normal serum fraction 90% 10%
Water solubility (polarity) 0 (non polar) + (polar)
Affinity to lipids (Kernicterus) +++ 
Renal excretion Nil +
Vanden Berg Reaction Indirect Direct
Temporary Albumin Binding +++ 0
Irreversible Delta Bilirubin 0 ++
What is the physiological
ANTI-OXIDANT
It’s an
function of BILIRUBIN ?
BILE SALT METABOLISM
CHOLESTEROL

CHOLIC ACID

PRIMARY BILE
LIVER ACIDS
CHENODEOXY CHOLIC
ACID

TAURINE / GLYCINE

CONJUGATED B A

DEOXYCHOLIC ACID DECONJUGATION

LITHOCHOLIC ACID

INTESTINE
JAUNDICE
 ETIOLOGY OF JAUNDICE

PRE-HEPATIC HEPATIC POST-HEPATIC

INCREASED DEFECTIVE
QUANTITY UPTAKE
MEDICAL
SURGICAL
JAUNDICE JAUNDICE
DEFECTIVE TRANSPORT BY
DEFECTIVE
BILIARY DUCT SYSTEM
DECREASED
DELIVERY TO LIVERCONJUGATION
DEFECTIVE
EXCRETION
 An Approach to Jaundice
• Is it isolated elevation of serum bilirubin ?
• is it unconjugated or conjugated fraction?
• Is it accompanied by other liver test
abnormalities ?
• Is the disorder hepatocellular or cholestatic?
• If cholestatic, is it intra- or extrahepatic?
• History and physical examination
• Interpretation of laboratory tests
• Radiological tests and procedures.
 BASIC LAB PARAMETERS
FOR WORKUP OF JAUNDICE

• BLOOD
BILIRUBIN
AMINOTRANSFERASES
ALKALINE PHOSPHATASE
GAMMA GLUTAMYL TRANSFERASE
5’ NUCLEOTIDASE
• URINE
BILE PIGMENTS
BILE SALS
UROBILINOGEN
 LFT’s

• Markers of hepatocellular damage

• Cholestasis

• Liver synthetic function

Markers of Hepatocellular damage
(Transaminases)

ALT

AST
 AMINOTRANSFERASES

ALT AST
• Cytosolic • 80% mitochondrial
• Quite liver • 20% cytosolic
specific • Not liver specific
• v.low • liver, heart skeletal
concentrations in muscle, kidneys,
kidney and brain, RBCs
skeletal muscles. • half-life 17hrs
• Half-life 47hrs
MARKERS OF CHOLESTASIS

GGT

ALP

5’ NUCLEOTIDASE
 GAMMA GLUTAMYL
TRANSPEPTIDASE
• hepatocytes and biliary epithelial cells,
pancreas, renal tubules and intestine
• Very sensitive but Non-specific
• Raised in ANY liver disease
hepatocellular or cholestatic
• Usefulness limited
 GAMMA GLUTAMYL
TRANSPEPTIDASE
• Confirm hepatic source for a raised
ALP
• Alcohol
• Isolated increase does not require any
further evaluation, suggest watch and
rpt 3/12 only if other LFT’s become
abnormal then investigate
 ALKALINE PHOSPHATASE
• Hepatic ALP present on surface of bile
duct epithelia
• accumulating bile salts increase its release
from cell surface.
• Takes time for induction of enzyme levels
• Elevation require de novo synthesis
• so may not be first enzyme to rise and
half-life is 1 week.
 ALP
• Large molecule size isoenzyme
appearing in cholestasis is of
hepatocyte origin
• attached to circulating membrane
fragments
• fragments contains other enzymes like
GGT, 5’NP & lipoprotein-X
• Occurs as a local effect of detergent
action of bile salts.
 ALP
• In biliary obstruction ALP reabsorbed
is in macromolecular form.
• Not readily excreted.
• CB is readily excreted.
• If some bileducts are obstructed
bilirubin can be normal whereas ALP is
elevated.
• Any infilterating lesion can produce
this picture.
 ALKALINE PHOSPHATASE

• ALP isoenzymes, 5-NT or gamma GT

may be necessary to evaluate the origin
of ALP
MARKERS IN ACUTE / TRANSIENT
CHOLESTASIS

TIME (days)
MARKERS IN CHRONIC CHOLESTASIS

TIME (weeks)
BIOCHEMICAL MARKERS IN
CHOLESTASIS
 5’ NUCLEOTIDASE

• Appears uniquely in liver disease

MARKERS OF SYNTHETIC
FUNCTION

BILIRUBIN
 Bilirubin testing

• Van den Berg Reaction

• SB + SAA  Diazo compound formed
• Diazo is chromogenic – Colourimerty
• Reaction in H2O medium – Direct – CB
• Reaction in ethnol medium – Indirect
• Indirect includes CB and UCB = Total B
• Time is the essence of the direct test
• Foam test, Ictotest for urine – CB only
 Normal values for LFT
Features
Total Bilirubin
Conjugated Bilirubin
AST (SGOT)
ALT (SGPT)
Alkaline phosphatase
GGT and 5’ Nucleosidase, CDT
Urine Bilirubin
Urine Urobilinogen
Urine Bile Salts
Healthy Normal
Less than 1.00 mg
Less than 0.15 mg
Less than 31 i.u/L
Less than 35 i.u/L
Less than 112 i.u /L
Significantly ↑ in ALD
Absent
In trace quantity
Absent
 Liver Function Tests (LFT)
Liver function test Normal Range Value
Bilirubin
Total 0.1 to 1.0 mg Dx. Of Jaundice,
Conjugated < 0.2 mg Severity
Alkaline phosphatase 25-112 iu/L Dx of Obstructive
Jaundice
Aspartate
transaminase 5-31 iu/L Early Dx and follow up
(AST/SGOT)
Alanine transaminase
5-35 iu/L AST/ALT > 1 in ALD
(ALT/SGPT)
Albumin 3.5-5.0 g/dL Assess severity of
disease
Prothrombin time (PT) 12-16 s Assess severity of
disease
 Utility of Liver Function Tests
LFT Utility of the test
ALT/SGPT ALT ↓than AST in alcoholism
Albumin Assess severity / chronicity
Alk. phosphatase Cholestasis, hepatic infiltrations
AST/SGOT Early Dx. of Liver disease, F/up
Bilirubin (Total) /Conjug. Diagnose jaundice

Gamma-globulin Dx. F/up Chronic hepatitis & cirrhosis

GGT Dx alcohol abuse, Dilantin toxicity

 Non Hepatic causes of abnormal LFT
Abnormal LFT Non hepatic causes
PLE, Nephrotic syndrome
Albumin
Malnutrition, CHF
Bone disease, Pregnancy,
AKP
Malignancy , Adv age
AST MI, Myositis, I.M.injections
Hemolysis, Sepsis,
Bilirubin
Ineffective erythropoiesis
Antibiotics, Anticoagulant,
PTT
Steatorrhea, Dietary
 Lab Diagnosis of Jaundice – D.D

Prehepatic Intrahepatic Posthepatic

Features
(Heamolytic) (Hepatocellular) (Obstructive)

Unconjugated ↑ Normal Normal

Conjugated Normal ↑ ↑
AST or ALT Normal ↑↑ Normal

Alkaline phos.
and GGT
Normal Normal ↑↑
Urine bilirubin Absent Present Increased

Urobilinogen Increased Present Absent

Algorithmic approach for Jaundice

How to clinically evaluate the patient ?

What tests will help us in D.D ?

What imaging modalities will be useful ?

How to monitor the progress ?

 First Step

Estimate Serum Bilirubin

Is it less than 1 mg % - Normal

Is it more than 1 mg % - Elevated

Second Step : If SB > 1.0 mg
Is it unconjugated bilirubin ?

Haemolytic Jaundice

Is it Conjugated Bilirubin ? (> 20%)

Hepatocellular jaundice

Obstructive jaundice
↑ in Unconjugated Bilirubin
Hemolytic Jaundice - Uncommon

1. Hemolytic Disorders + Anemia

Inherited – Sphero, SS, G6PD, PK

Acquired – MAHA, PNH

2. Ineffective Erythropoesis –B12, Fe, F

3. Drugs – Rifampicin, Probenecid

4. Inherited –Crigler Najjar, Gilberts

Third Step : If CSB is increased
Do - AST and ALT (SGOT and SGPT)

Elevated AST and ALT

Hepatocellular jaundice

AKP, 5N, GGT will be normal

Do - Alkaline Phosphatase and GGT

AKP, GGT ↑↑ in Obstructive Jaundice

AST and ALT will be normal

Fourth Step : Hepatocellular
Hepatocellular – Features and D.D

Conjugated SB is increased
AST and ALT are increased
AKP, 5NS, GGT are normal
Hepititis – A,B,C,D,E, CMV,EBV

Toxic Hepatitis – Drugs, Alcohol

Malignancy – Primary Ca
Cirrhosis – ALD, NAFLD
Cholestatic jaundice
 Cholestasis
• symptom of many diseases.
• defined as a pathologic state of reduced
bile formation or flow.
• This definition applies more to the
experimental situation, where the rates of
bile formation and flow can be measured,
than to human cholestasis, where neither
can be assessed.
 CHOLESTASIS

“BILE SECRETORY FAILURE OF

THE LIVER CELL WITH
CONCOMITANT ACCUMULATION
OF BILE CONSTITUENTS IN THE
BLOOD.”

Desmet et al 1979
Clinical definition of cholestasis

• any condition in which substances

normally excreted into bile are retained.
• The serum concentrations of
conjugated bilirubin and bile salts are
the most commonly measured.
 mechanisms of cholestasis

• Hepatocellular  where an impairment

of bile formation occurs

• Obstructive  where impedance to bile

flow occurs after it is formed.
 histopathologic features
• hepatocellular cholestasis presence of
bile within hepatocytes and canalicular
spaces, in association with generalized
cholate injury.
• obstructive cholestasis  bile plugging of
the interlobular bile ducts, portal expansion,
and bile duct proliferation in association with
centrilobular cholate injury.
PATHOPHYSIOLOGICAL
CHANGES & BASIS OF
SYMPTOMS
 In theory

• Impairment of hepatocyte function

should impair bilirubin conjugation
• Cholestasis within cholangioles should
not affect bilirubin conjugation
 BUT

• Close juxtaposition of both cell types in

liver arhitecture ensures that diseases
of the intrahepatic biliary tree & of
hepatocytes usually affect each others
function.
 PARADOX OF RAISED
FRACTIONS OF BILIRUBIN

• Thus pathology in liver results in

increase of both conjugated &
unconjugated bilirubin irrespective of
wheather the primary insult is to
hepatocytes or cholangioles
 AMPLIFICATION OF
PATHOLOGICAL EVENTS
• There are multiple pathways for
bilirubin transport
• Effect of single point obstruction will
produce only subtle symptoms of
cholestasis.
• For a picture of full blown cholestasis
amplification mechanisms are needed.
 amplification mechanisms -1
retained bile salts
• retention of hydrophobic bile salts,
strong detergents that cause
membrane injury and impairment of
membrane function.
• Retained bile salts down-regulate new
bile acid synthesis  reduction of the
bile salt pool  reduced Enterohepatic
recirculation.
 amplification mechanisms -2
retention of cholesterol

• increased cholesterol content of

membranes
 that reduces their fluidity
impairs the function of
integral membrane proteins
 result of amplification
mechanisms
• retention of damaging substances

• accelerated membrane injury

• dysfunction

• generalized failure of the excretory

mechanism for bile
 result of amplification
mechanisms

• This converging pathway

makes the differentiation of
cholestatic diseases on clinical
grounds very difficult.
 Retention of conjugated bilirubin
and its regurgitation into serum
• Excretion of conjugated bilirubin is the
rate-limiting step of bilirubin clearance.
• During cholestasis, conjugation of
bilirubin continues but excretion is
reduced.
• The mechanism by which conjugated
bilirubin regurgitates into serum may
differ according to the disease etiology.
 Retention of conjugated bilirubin
and its regurgitation into serum
• In hepatocellular cholestasis, where
bile formation is reduced, conjugated
bilirubin is likely to efflux directly from
the hepatocyte via diffusion or
vesicular exocytosis.
• in obstructive cholestasis, conjugated
bilirubin possibly enters the canalicular
space and effluxes back through a
weakened tight junction.
Retention of conjugated bilirubin and its
regurgitation into serum

The magnitude of elevation is not

diagnostically important because it
does not reflect the type or degree of
cholestasis.
 For example………………
• investigations clearly indicate that
patients with neonatal giant cell
hepatitis typically have more bile flow
than patients with biliary atresia
• BUT….the serum conjugated bilirubin
concentration is usually higher in
neonatal giant cell hepatitis.
• this probably reflects an increase in
bilirubin production.
Retention of conjugated bilirubin and its
regurgitation into serum
• The presence of elevated serum
concentration of conjugated bilirubin is
a principal sign of cholestasis.

• It results in jaundice, which can be

detected by scleral icterus at a
concentration as low as 2 mg/dL, and
by dark urine
Retention of conjugated bilirubin and its
regurgitation into serum
• Alternate elimination pathways, principally
by way of the kidneys, limit the absolute
elevation of conjugated bilirubin.
• Conjugated bilirubin concentration rarely
exceeds 30 mg/dL, although such elevated
levels can occur.
• Because conjugated bilirubin is relatively
weakly bound to albumin, it can dissociate
relatively easily and be filtered into the urine.
Retention of conjugated bilirubin and its
regurgitation into serum
• Newer methods have resulted in the
discovery of a fraction of serum bilirubin that
is covalently bound to albumin, known as
delta bilirubin or biliprotein.
• This complex is formed in plasma by a
nonenzymatic process.
• The presence of large quantities of delta
bilirubin indicates long-standing cholestasis.
 DELTA BILIRUBIN

the cause for

persistence of
jaundice even after
relief of biliary
obstruction.
 Hypercholemia
• the liver cell retains bile salts, resulting
in down-regulation of new bile acid
synthesis
• overall reduction in the total pool size.
• Bile salts are regurgitated from the
hepatocyte,  increase in the
concentration of bile salts in the
peripheral circulation.
 Hypercholemia
uptake of bile salts entering the liver in
portal vein blood is inefficient

spillage of bile salts into the peripheral

circulation
 pruritis
• Newer theories suggest that patients
have differing sensitivities to elevated
bile salt concentrations  act on
peripheral pain afferent nerves 
produce the sensation of itching.

• involves opiate-mediated pathways

 pruritis

• opiate antagonists can block

cholestasis-associated itching.

• Itching does not appear to be

associated with histamine release, and
antihistamine therapy is generally
ineffective.
 Hyperlipidemia
• Bile is the normal excretory pathway for
cholesterol, and with reduced bile
formation, cholesterol is retained.

• Cholesterol retention can cause an

increase in membrane cholesterol content
and a reduction in membrane fluidity and
membrane function, thereby amplifying
the cholestasis
 Hyperlipidemia

• plasma cholesterol is in the form of

lipoprotein-X, an abnormal lipoprotein
observed only in the serum of patients
with cholestasis.
 Hyperlipidemia
• often exceeds 1,000 mg/dL and
sometimes can be as high as 4,000
mg/dL
• does not have as great an effect on the
cardiovascular system.
• lipoprotein-X,lacks the surface protein
constituents necessary to interact with
vascular endothelium.
 Xanthomas
• result from the deposition of cholesterol
into the dermis.
• development of xanthomas is more
characteristic of obstructive cholestasis
than of hepatocellular cholestasis.
• may develop rapidly over a few months in
acute extrahepatic biliary obstruction
 Xanthomas
• Acutely developing xanthomas are usually the
eruptive type, which are white pustular lesions,
pinpoint to 2 mm in diameter, that appear first on the
trunk and in the diaper area.
• Planar xanthomas occur first around the eyes but
also in the creases of the palms,soles and on the
neck develop more slowly and are principally
observed in chronic cholestasis syndromes.
• tuberous xanthomas are associated with very long
duration of cholestasis and develop over the
extensor surfaces, such as the elbows, Achilles
tendons, and knees.
 failure to thrive
• mechanisms of failure to thrive include
malabsorption
anorexia
poor nutrient use
hormonal disturbances
secondary tissue injury
EXTRAHEPATIC – BILIARY
OBSTRUCTION
 CAUSES

• WITHIN THE LUMEN

• WALL
• COMPRESSION FROM OUTSIDE
WITHIN THE LUMEN

• Gall stones
• Cystic fibrosis
• Parasites
• hemobilia
Affecting wall of bile duct

• Biliary malformation
• Iatrogenic division
• Cholangio carcinoma
• Sclerosing cholangitis
• c/c pancreatitis
COMPRESSION FROM OUTSIDE

• Tumours
• Peritoneal adhesions
• Retroperitoneal cysts
• Hepatic artery aneurysm
• Duodenal diverticulum
Aetiology according to site of
biliary obstruction
 Intrahepatic
bile ducts

Hepatic ducts
Biliary
CBD tree in
relation to
Gall bladder pancreas

duodenum
Intrahepatic bile ducts

• Liver tumors
• Cholangitis
• Hemobilia
• Caroli’s disease
Hepatic ducts

• Cholangiocarcinoma
• Choledocholithiasis
• Biliary atresia
 Gall bladder

• Ca gallbladder
• Gall stones (Mirizzi’s syndrome type IV)
 CBD

• Choledocholithiasis
• Cholangiocarcinoma
• Choledochal cyst
• CBD stricture
• Sclerosing cholangitis
 Biliary tree in relation to
pancreas

• Carcinoma head of pancreas

 Duodenal causes

• Ampullary tumor
• Duodenal diverticula
• Inflammatory bowel disease
 Clinical features

• Features of cholestasis
• Features of Cholangitis
• Features of the primary causative
pathology
• Late features
 Features of cholestasis
Early  jaundice
dark urine
pale stools
pruritis

Late  xanthelesma
xanthoma

Malabsorption weight loss

steatorrhoea
hepatic osteodystrophy
bleeding tendancy
 Features of Cholangitis

Charcot’s triad fever with rigors

pain
jaundice

Reynolds's pentad Charcot’s triad

shock
CNS depression
Features of the primary causative
pathology
• Palpable mass p/a
• Palpable GB
• Palpable Pancreatic mass
• Ascitis
• Murphy’s sign
• Boa’s sign
 Late features
• Features of c/c liver disease
palmar erythema,spider naevi,…..etc

• Features of Impending liver failure

incoordination,asterexis…………..etc

• Features of malignancy
weight loss, Troisier’s sign,……….etc
CAN HISTORY & PHYSICAL
EXAMINATION SUGGEST A WORKING
DIAGNOSIS
 JAUNDICE IN SURGICAL
PATIENTS
I- NEOPLASTIC JAUNDICE
Ca HOP, periampulary Ca
Ca GB, HCC with secondaries

II - CALCULOUS JAUNDICE

III - OTHER CAUSES

 Suggesting malignancy
• Relentlessly progressive steadily deepening
obstructive jaundice, weight loss.

• A palpable gall-bladder felt as an elongated,

smooth, non-tender mass, normal in contour,
and slightly mobile, which may extend to the
patient's umbilicus or even below it.

• If gall-bladder distended , it strongly

suggests a malignant obstruction at the
lower end of common bile-duct, but its
absence does not exclude this.
 Suggesting secondary deposits in liver

• large, knobbly liver

 Suggesting a carcinoma of
stomach with secondaries in porta
• Hepatis
• pain
• Anorexia
• Vomiting
• upper abdominal mass
• visible peristalsis of pyloric stenosis.
• Anaemia
Suggesting carcinoma of the
head of his pancreas

• vague epigastric pain

• weight loss.
• Palpale GB
 Suggesting gallstones
• a long history of intermittent varying
jaundice,
• severe intermittent colicky pain
• non-palpable gall-bladder
• fever, chills, and rigors (suggesting
cholangitis)
• little or no weight loss
• flatulent dyspepsia
• raised white count suggests cholecystitis.
 Suggesting hepatoma

• large, hard, irregular liver.

• bruit is often present
• ascites is common & often
bloodstained.
 Suggesting stenosis

• tender, enlarged liver

• gall-bladder may or may not be
palpable.
Suggesting carcinoma of the
gall-bladder

• enlarged liver
• hard, irregular mass in
right hypochondrium
Thank
you